Adaptation ofSaccharomyces cerevisiaeto the Herbicide 2,4-Dichlorophenoxyacetic Acid, Mediated by Msn2p- and Msn4p-Regulated Genes: Important Role ofSPI1

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Abstract
The possible roles of 13 Msn2p- and Msn4p-regulated genes in the adaptation ofSaccharomyces cerevisiaeto the herbicide 2,4-d-dichlorophenoxyacetic acid (2,4-D) were examined. Single deletion of genes involved in defense against oxidizing agents (CTT1,GRX1, andGRX2/TTR1) or encoding chaperones of the HSP70 family (SSA1,SSA4, andSSE2) showed a slight effect. A more significant role was observed for the heat shock genesHSP78,HSP26,HSP104,HSP12, andHSP42, most of which encode molecular chaperones. However, theSPI1gene, encoding a member of the glycosylphosphatidylinositol-anchored cell wall protein family, emerged as the major determinant of 2,4-D resistance.SPI1expression reduced the loss of viability of an unadapted yeast population suddenly exposed to the herbicide, allowing earlier growth resumption. Significantly, yeast adaptation to 2,4-D involves the rapid and transient Msn2p- and Msn4p-mediated activation (fivefold) of SPI1transcription.SPI1mRNA levels were reduced to values slightly above those in unstressed cells when the adapted population started duplication in the presence of 2,4-D. SinceSPI1deletion leads to the higher β-1,3-glucanase sensitivity of 2,4-D-stressed cells, it was hypothesized that adaptation may involve an Spi1p-mediated increase in the diffusional restriction of the liposoluble acid form of the herbicide across the cell envelope. Such a cell response would avoid a futile cycle due to acid reentry into the cell counteracting the active export of the anionic form, presumably through an inducible plasma membrane transporter(s). Consistent with this concept, the concentration of14C-labeled 2,4-D in 2,4-D-energized adapted Δspi1mutant cells and the consequent intracellular acidification are higher than in wild-type cells.

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